O'Shaughnessy C T, Connor H E, Feniuk W
Department of Neuropharmacology, Glaxo Group Research Ltd, Ware, UK.
Cephalalgia. 1993 Jun;13(3):175-9; discussion 149. doi: 10.1046/j.1468-2982.1993.1303175.x.
The aim of this study was to investigate the effect of the anti-migraine drug and selective 5-HT1 receptor agonist, sumatriptan, on membrane potential of guinea-pig isolated trigeminal ganglion. Ganglia were divided into three longitudinally, placed in two-compartment baths and the d.c. potential between compartments was recorded extracellularly. Drugs were applied to the Krebs superfusion fluid of one compartment. KCl (3 mmol/l) and GABA (0.1 mmol/l) caused depolarization (0.30 +/- 0.05 and 0.55 +/- 0.08 mV respectively, n = 11-19). 5-HT (1-10 mumol/l) caused small depolarizations (0.06 +/- 0.02 mV, n = 8) but sumatriptan (0.1-10 mumol/l) had no effect on trigeminal ganglion membrane potential. Collagenase pretreatment, to enhance desheathing, or modification of the composition of the Krebs solution failed to reveal any effect of sumatriptan. These data provide no evidence to suggest that sumatriptan inhibits neurotransmission in trigeminal ganglion. However, 5-HT1 receptors may be present in insufficient numbers in the trigeminal ganglion to elicit a change in membrane potential. Further studies are required to investigate the effect of sumatriptan at the level of the sensory nerve terminals within the intracranial vasculature, where 5-HT1 receptors may be concentrated.
本研究旨在探讨抗偏头痛药物及选择性5-羟色胺(5-HT)1受体激动剂舒马曲坦对豚鼠离体三叉神经节膜电位的影响。将神经节纵向分为三份,置于双室浴槽中,细胞外记录两室之间的直流电位。将药物应用于其中一室的 Krebs 灌流液中。氯化钾(3 mmol/L)和γ-氨基丁酸(GABA,0.1 mmol/L)引起去极化(分别为0.30±0.05和0.55±0.08 mV,n = 11 - 19)。5-羟色胺(1 - 10 μmol/L)引起小幅度去极化(0.06±0.02 mV,n = 8),但舒马曲坦(0.1 - 10 μmol/L)对三叉神经节膜电位无影响。用胶原酶预处理以增强脱鞘作用,或改变 Krebs 溶液的成分,均未能显示舒马曲坦有任何作用。这些数据没有提供证据表明舒马曲坦抑制三叉神经节中的神经传递。然而,三叉神经节中5-HT1受体的数量可能不足以引起膜电位的变化。需要进一步研究来探讨舒马曲坦在颅内血管内感觉神经末梢水平的作用,5-HT1受体可能在那里聚集。